LETTERS 1317

concurrent with a defective response to IL-1 by their T lymphocytes, partictllarly by those of patients whose mono- cytes spontaneously produced IL-I .

It would therefore seem that scleroderma patients, who JSO have been shown to have increased function of T helper cells (4-6), a T cell subpopulation particularly respon- sive it0 IL-1 (7), and an early proliferative response in autologous mixed lymphocyte reactions (8), have, as an important pathogenetic factor, increased in vivo production of mcinokines, including IL-1. This could cause fibroblast proliferation and increased synthesis of both collagen (9) and glycosaminoglycan (1).

Donato Alarc6n-Segovia, MD Jorge Alcocer-Varela, MD Instituto Nacional de la Nutricibn

Salvador Zubirtin Mexico City, Mexico

1. Whiteside TL, Worrall JG, Prince RK, Buckingham RB, Rodnan GP: Soluble mediators from mononuclear cells increase the synthesis of glycosaminoglycan by dermal fibroblast cultures derived from normal subjects and progressive systemic sclerosis patients. Arthritis Rheum 28: 188-197, 1985

2. Schmidt JA, Mizel SB, Cohen D, Green I: Interleukin 1, a potential regulator of fibroblast proliferation. J Immunol

3. Alcocer-Varela 3, Martinez-Corder0 E, Alarc6n-Segovia D: Spontaneous production of, and defective response to, interleu- kin- I by peripheral blood mononuclear cells from patients with scleroderma. Clin Exp Immunol 59:666-672, 1985

4. Alarc6n-Segovia D, Palacios R, Ibafiez de Kasep G: Human post-thymic precursor cells in health and disease. VIII. Immuno- regulatory circuits of the peripheral blood mononuclear cells fromi patients with progressive systemic sclerosis. J Clin Lab Immunol5:143-148, 1981

5 . Inoshita T, Whiteside TL, Rodnah GP, Taylor FH: Abnormali- ties of T lymphocyte subsets in patients with progressive system- ic sclerosi; (PSS, scleroderma). J Lab Clin Med 97:264-277, 1981

6. Krakauer RS, Sundeen J, Sauder DN, Scherbel A: Abdormalities of inimunoregulation in progressive systemic sclerosis: evidence for excess helper cell function and altered B cell function. Arch Demnatol 117:80-82, 1981

7. Fishlbein E, Alcocer-Varela J, Alarc6n-Segovia D: Cellular bases of the production of and response to interleukin-2 in man: role of autollogous rosette-forming T-cell subsets defined with monoclo- nal antibodies. Immunology 50:223-227, 1983

8. Alcocer-Varela J, Laffon A, Alarcbn-Segovia D, Ibafiez de Kasep G: Early proliferative response in the human autologous mixed lymphocyte reaction in scleroderma. J Rheumatol 11:48- 52, 1984

9. GonzAlez-Amaro R, Alarc6n-Segovia D, Alcocer-Varela J, Diaz- De-L.e6n L: Mononuclear cell-fibroblast interactions in sclero- derma. Submitted for publication

128: 2 177-2 182, 1982

Is primary chronic uveitis responsive to treatment with nonsteiroidal antiinflammatory drugs? To the Editor:

We have read with great interest the article by Wakefield et al (1) on HLA-B27 and alphal-antitrypsin in patients with chronic primary uveitis. The relationship be- tween this disease and alpha,-antitrypsin level has been explored by others as well (2).

With the rationale that patients with chronic primary uveitis have a relative protease excess due to low levels of alphal-antitrypsin (3), we have tried to stop the inflamma- tory process by using eaminocaproic acid.

We describe 1 of our patients, a 52-year-old white woman who, for 2 years, had chronic primary uveitis that was resistant to local and systemic treatment with steroids. She was HLA-B27 negative and her level of alpha,-antitryp- sin was 160 mg/ml (normal 240-370).

After 30 days of treatment with .s-aminocaproic acid, the patient had complete clinical remission of her symptoms. After discontinuation of the treatment for 7 days, she developed a flare of the disease, which was controlled after a second trial with the same drug.

These findings have prompted us to develop a con- trolled trial to demonstrate the effectiveness of s-aminoca- proic acid in the treatment of chronic primary uveitis.

G. P. Astorga, MD, FACP M. T. Cuchacovich, MD University of Chile School of Medicine Santiago, Chile

1. Wakefield D, Breit SN, Clark P, Penny R: Immunogenetic factors in inflammatory eye disease: influence of HLA-B27 and alpha,-antitrypsin phenotypes on disease expression. Arthritis Rheum 25:1431-1434, 1982

2. Brown WT, Mamelok AE, Beam AG: Anterior uveitis and alpha 1 antitrypsin (letter). Lancet 1:646, 1979

3. Morse JO: Alpha 1-antitrypsin deficiency. N Engl J Med 299: 1045-1048, 1978

Poe’s finger: the tell-tale digit To the Editor:

It is widely known that cold can precipitate episodes of Raynaud’s phenomenon, blanching of a digit succeeded by cyanosis and sometimes hyperemia. That psychological stress may be another cause of this phenomenon has also been observed. This is illustrated by the clinical pattern of a patient recently seen by us.

A 61-year-old man noted the initial manifestation of his illness 40 years ago. The first evidence was that he consistently lost money in poker games. Later, a friend called attention to the fact that his fingers would blanche when he was dealt a winning hand. Consequently, the other players had quickly learned not to bet when his fingers were white.

Twenty years later he developed the other features of the CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias), as well as discharge of gritty material from the skin, dyspha- gia, thickening and tightness of the digital skin, arthralgias, moderately severe restrictive lung disease, impotence, and arrhythmias.

Clearly, the digital blanching was due to Raynaud’s phenomenon induced by the psychological stress of being

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dealt winning cards. This interesting and unusual circum- stance deserves a memorable name. Among those consid- ered were “poker player’s handicap,” “tattling digit syndrome,” and “Raynaud’s revenge.” Since there is a similarity to the murderer who became pale and developed severe palpitations under psychological stress in Edgar Allen Poe’s short story, “The Tell-Tale Heart” (Poe EA: Tales of Mystery and Imagination. New York, Weathervane Books, 1935), we prefer to call this condition “Poe’s finger: the tell- tale digit.” The name is particularly appropriate since the patient who manifested the condition was seen in Richmond, the childhood home of Poe.

Elam Toone, MD George F. Moxley, MD David M. Hudgins, MD Medical College of Virginia McGuire Veterans Administration

Richmond, VA Medical Center

Comment on article by Husby and Williams To the Editor:

We read with interest the article by Husby and Williams (1) on the immunohistochemical studies of interleu- kin-2 (IL-2) and y-interferon in rheumatoid arthritis (RA) synovial tissue. The authors refer to our finding that IL-2- dependent T cells are detectable in the synovial fluids of RA patients (2) and mention that interleukin-1, which has also been demonstrated in such fluids (3), acts as a stimulus for IL-2 production. We would like to point out that we have also found IL-2-like activity in synovial fluids of 12 of 14 RA patients studied (4), but not in degenerative or traumatic joint disease fluids, as detected by the IL-2-dependent murine T cell line, CT-6.

One of the problems of demonstrating this IL-2 activity was the presence of a high molecular weight inhibi- tor, which had to be inactivated or diluted out before IL-2 was detectable. These findings would certainly suggest that IL-2-producing cells are present in the synovial environ- ment. We were similarly able to demonstrate interferon (IFN) activity in RA synovial fluids, using a functional viral- inhibition test system, in 22 of 31 samples tested.

In contrast, when the lymphokine-producing capabil- ities of IL-2-dependent T cell clones derived from synovial fluids and tissues were examined, a dissociation between IL- 2 and IFN was noted; all T cell clones tested, no matter what their phenotype, released IFN in response to mitogen stimu- lation, whereas none of these clones produced IL-2. Of course, this dissociation may simply reflect an in vitro selection process for IL-2 dependency, rather than a specific defect in IL-2 production or in vivo selection. However, we have some evidence that T cell lines generated from the

synovial environment are better able to proliferate in re- sponse to IL-2-containing synovial fluids than are IL-2- dependent lines generated similarly from peripheral blood (5).

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Richard J. Warrington, MB, BS, PhD Rachel McKenna, PhD William Ofosu-Appiah, MSc John A. Wilkins, PhD University of Manitoba Winnipeg, Manitoba, Canada

Husby G, Williams RC Jr: Immunohistochemical studies of interleukin-2 and yinterferon in rheumatoid arthritis. Arthritis Rheum 28:174-181, 1985 Wilkins JA, Warrington RJ: The generation of interleukin-2 dependent continuous T cell lines from synovial fluid mono- nuclear cells in rheumatoid arthritis (abstract). Clin Res 30:810A, 1982 Fontaine A, Hengartner H, Weber E, Fehr K, Grob PJ, Cohen G: Interleukin 1 activity in the synovial fluid of patients with rheumatoid arthritis. Rheumatol Int 2:49-53, 1982 Wilkins JA, Warrington RJ, Sigurdson SL, Rutherford WJ: The demonstration of an interleukin-2 like activity in the synovial fluids of rheumatoid arthritis patients. J Rheumatol 10: 109-1 13, 1983 Wilkins JA, Olivier SL, Warrington RJ: Generation of interleu- kin-2-dependent T cell lines from synovial fluids in rheumatoid arthritis. Clin Exp Immunol 58: 1-6, 1984

Regulation of susceptibility to bacterial cell wall-induced arthritis in rats To the Editor:

Chronic proliferative and erosive synovitis can be induced in rats by systemic injection of an aqueous suspen- sion of cell wall fragments from selected bacteria such as Streptococcus pyogenes, group A or Lactobacillus casei (1,2). This experimental model exhibits many of the clinical, pathologic, and immunologic features of rheumatoid arthritis and various other inflammatory arthritides, and thus pro- vides an experimental system to explore mechanistic ques- tions relevant to human disease. We have been particularly interested in defining mechanisms that regulate susceptibil- ity and resistance to chronic disease in this experimental model.

We have previously demonstrated that following an intraperitoneal injection of an aqueous suspension of cell wall fragments from group A streptococci into LEW/N female rats, the cell wall fragments disseminate to and persist in synovial tissues of peripheral joints (3). The localization of cell wall antigens to synovial tissues in this strain of rats is associated with the development of severe, chronic, proliferative and erosive synovitis. In the same study, we were able to obtain only equivocal evidence, by immunofluorescence techniques, of cell wall antigens in the synovium of chronic arthritis-resistant F344/N female rats.

Prompted by our observations that l4C-radio1abeled cell wall fragments from L casei disseminate to and persist in